[The relationship between students' well-being and their parents' knowledge and support in a metropolitan area].

OBJECTIVES: The purpose of this study was to clarify the causal relationship between students' well-being and their parents' knowledge and support in raising them in a prefecture by using covariance structural analysis. METHODS: In November 2007, a questionnaire survey was conducted with 11,363 elementary school students (4th grade),junior high school students (1st grade) and high school students (1st grade) as well as their parents. The total number of responses analyzed were 9,651 pairs of matched data for parents and their children. RESULTS: A concept model was proposed to use four latent variables determined by factor analysis. "Students' well-being" (" " means latent variable) classified as a latent variable, was not prescribed directly by "parents' knowledge and support", but rather developed indirectly through "physical activities" and "communication between the students and parents". The decision coefficients for the students' well-being determined with this model ranged from 27% to 40%. Depending on the participant's age and gender, they were divided into six groups. CONCLUSION: This study indicated that positive support for children's health and well-being by the parents was important for students to have a happy and healthy lifestyle. It became structurally clear that it was necessary for both students and their parents to engage in physical activities and have good communication with each other in order to stimulate and develop children's health practice and well-being.

Tissue factor pathway inhibitor production by human proximal tubular epithelial cells in culture.

Fibrin deposition in the peritubular capillaries and along the tubular basement membrane is commonly observed in several renal diseases and suggests the involvement of blood coagulation in tubulointerstitial damage. It has been demonstrated that tissue factor (TF) is present in tubular epithelial cells of animal models of nephritis. Tissue factor pathway inhibitor (TFPI) regulates the extrinsic pathway of blood coagulation through its ability to inhibit TF activity and it is now thought to be produced mainly by the vascular endothelial cells. We examined whether human proximal tubular epithelial cells (PTEC) could produce TFPI and attempted to clarify the regulatory factors affecting TFPI production. Cultured human PTEC were used. The procoagulant activity (PCA) in PTEC lysate was quantified by measurement of the one-stage recalcification time. TFPI in the cell supernatants was measured by ELISA. The mRNA of TF and TFPI in PTEC was analyzed by reverse transcriptase polymerase chain reaction (RT-PCR). PCA which is compatible with TF activity was present in the PTEC lysate. TF mRNA and TFPI mRNA were detected in PTEC. The amount of TFPI increased over time in the cell supernatants. Immnoblot analysis revealed 40 kD protein of TFPI, and TFPI antigen was demonstrated in PTEC by immunofluorescence. The concentration of TFPI was significantly increased following incubation with thrombin and heparin in a dose- and time-dependent manner, although the amount of TFPI mRNA was not changed. Our study showed that TFPI is produced in cultured PTEC and added one more cell type that produced TFPI other than endothelial cells. Thrombin and heparin stimulated TFPI secretion from PTEC. TFPI of PTEC may act against generation of thrombin and tubular fibrin formation induced by tissue factor activation. The augmentation of TFPI secretion by heparin may play an important role in the modulation of anticoagulant properties of PTEC.

Effects of eparlestat on plasma levels of advanced glycation end products in patients with type 2 diabetes.

Advanced glycation end products (AGE) are produced by a nonenzymatic reaction between glucose and proteins in the plasma of diabetic patients. Recently, AGE have been reported to promote and accelerate diabetic complications and atherosclerosis. The activity of aldose reductase (AR) is increased in diabetic patients. AGE are reported also to be produced by increased levels of fructose through increased activity of AR in diabetes. Consequently, we administered eparlestat, one of AR inhibitors, to diabetic patients and investigated the plasma carboxymethyl-lysine (CML) concentration, one of the AGE, before and after the administration of eparlestat. Though plasma CML concentration did not show any significant changes in all patients after the administration of eparlestat in the present study (from 2.7 +/- 0.3 mU/mL to 2.5 +/- 0.2 mU/mL; 3 months, 2.9 +/- 0.3 mU/mL; 6 months), plasma CML concentration were significantly decreased 3 months after the administration of eparlestat in the patients whose CML concentration before the treatment was higher than 3 mU/mL (from 3.4 +/- 0.2 mU/mL to 2.6 +/- 0.2 mU/mL; 3 months, p = 0.017). Serum thrombomodulin and HbA1c levels did not show any significant changes. These results suggest that the administration of eparlestat may be beneficial in preventing diabetic complications by decreasing plasma CML in diabetic patients.

Glial fibrillary acidic protein is one of the key factors underlying neuron-like elongation in PC12 cells.

Nerve growth factor (NGF) normally induces the differentiation of PC12 cells into a neuron-like phenotype. In this study, we found that exposure of PC12 cells to a temperature of 42°C for 24 h significantly decreased NGF-induced neurite elongation. Glial fibrillary acidic protein (GFAP) levels were decreased when PC12 cells were exposed to the heat stress, while PC12 cells overexpressing the gene encoding GFAP showed resistance. Mock-transfected PC12 cells exposed to NGF could be cultured for 72 h at 37°C, whereas GFAP-transfected PC12 cells exposed to NGF could be cultured for over 100 h. Our results suggest that GFAP is necessary for the long-term maintenance of cells with a neuron-like phenotype.

Poloxamer 188 enhances apoptosis in a human leukemia cell line.

Poloxamer block copolymers have been studied in multiple applications as drug delivery systems (DDS). These A-B-A amphiphilic block copolymers up-regulate the expression of selected genes in cells and alter genetic responses to antineoplastic agents in cancer. One example is poloxamer 188, also known as pluronic F68, which may be promising as a carrier in DDS. To clarify the possible mechanistic role of pluronic F68 in several leukemia cell lines, we examined whether pluronic F68-inducible factors were capable of causing apoptosis. The influence of pluronic F68 on the cell lines was examined using a comprehensive analysis. It was found that treatment of K562 cells with 6% pluronic F68 resulted in G2/M phase arrest of the cell cycle, followed by caspase activation and the accumulation of apoptotic cells. When used as a carrier in a DDS, pluronic F68 may provide a synergistic effect on the drug of interest. Although the mechanisms behind the function of pluronic F68 are not fully understood, the results suggests that pluronic F68 may act as a useful carrier in DDS for the purpose of leukemia therapy.

Thrombin stimulates production of fibronectin by human proximal tubular epithelial cells via a transforming growth factor-beta-dependent mechanism.

BACKGROUND: Tubulointerstitial fibrosis contributes to the progression of many forms of glomerular disease and to end-stage renal failure. Inflammatory mediators generated during glomerular injury may induce tubulointerstitial lesions by stimulating tubular cells. Thrombin has multiple biological functions in addition to its role in haemostasis and has been detected in the urine of patients with glomerular diseases. The present study investigated whether thrombin can modulate the production of fibronectin (FN) in cultured human proximal tubular epithelial cells (PTEC). METHODS: Cultured PTEC were incubated with or without thrombin to examine the effect of thrombin on FN production in PTEC. FN and transforming growth factor-beta (TGF-beta) levels were measured in culture supernatants by enzyme-linked immunosorbent assay (ELISA). Expression of FN mRNA was analysed by reverse transcriptase-polymerase chain reaction. Effects of thrombin on matrix metabolism were examined by enzyme immunoassay for the detection of secreted matrix metalloproteinase (MMP) and its inhibitors (TIMPs) as well as by zymography. RESULTS: Thrombin stimulated FN secretion in PTEC. Thrombin also stimulated TGF-beta secretion in PTEC in a dose-dependent manner. Expression of FN mRNA by PTEC was augmented by thrombin. The stimulatory effect of thrombin on FN secretion was inhibited by neutralizing antibodies against TGF-beta but not by an irrelevant antibody. Thrombin-induced FN secretin was also inhibited by thrombin inhibitors, such as antithrombin III, hirudin and argatroban. Although thrombin stimulated TIMP-1 and -2 secretion by PTEC, the stimulatory effect of thrombin on MMP-2 was not statistically significant. Thrombin did not affect the expression of MMP-2 in zymography studies. CONCLUSIONS: We found that thrombin stimulates FN production in PTEC without causing matrix degradation, an effect that may contribute to the formation of tubulointerstitial fibrosis associated with glomerular disease. The stimulatory effect of thrombin on FN production in PTEC is, at least in part, mediated by TGF-beta.